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Medicine Cardiovascular > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What are arrhythmias?

A

Disturbances in heart rate or rhythm that can be caused by changes in impulse formation or impulse conduction

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2
Q

Where do supraventricular arrhythmias arise?

A

In the atria or AV node

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3
Q

Where do ventricular arrhythmias arise?

A

In the ventricles

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4
Q

What do alterations in impulse formation involve?

A

Changes in automaticity, triggered activity

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5
Q

What do abnormalities in impulse conduction arise from?

A

Re-entry, conduction block, accessory tracts

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6
Q

Rate of pacemaking in the AV node

A

50-60bpm

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7
Q

Rate of pacemaking in the purkinje fibres

A

30-40bpm

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8
Q

Overdrive suppression

A

The SA node pacemaking is the highest and is dominant over other latent pacemakers

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9
Q

What happens if overdrive suppression is lost?

A

That triggers the latent pacemakers to take over

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10
Q

What can cause loss of overdrive suppression?

A

SA node firing frequency is pathologically low, conduction of impulse from SA node is impaired, if a latent pacemaker fires at an intrinsic rate faster if SA node despite SA node functioning normally, as a response to tissue damage

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11
Q

Ectopic beat

A

A heartbeat due to an impulse generated somewhere in the heart outside the AV node. A series of these can generate an ectopic rhythm

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12
Q

What things can cause an ectopic rhythm?

A

Ischaemia, hypokalaemia, increased sympathetic activity, fibre stretch

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13
Q

Afterdepolarisations

A

When a normal action potential triggers abnormal oscillations in the membrane potential

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14
Q

Two types of afterdepolarisations

A

Early afterdepolarisations and delayed afterdepolarisation

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15
Q

When do early afterdepolarisations occur?

A

During the inciting action potential within late phase 2 (terminal plateau) and early phase 3 (partial repolarisation occurring)

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16
Q

What are early afterdepolarisations occurring in late phase 2 mediated by?

A

Calcium channels when sodium channels are still closed

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17
Q

What are early afterdepolarisations occurring in early phase 3 mediated by?

A

Sodium channels

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18
Q

When are early afterdepolarisations most likely to occur?

A

When heart rate is low

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19
Q

What are early afterdepolarisations associated with?

A

Purkinje fibres, prolongation of the action potential and drugs that prolong the QT interval

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20
Q

When do delayed afterdepolarisations occur?

A

After complete repolarisation

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21
Q

What are delayed afterdepolarisations caused by?

A

Large increases in calcium

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22
Q

How do large increases in calcium result in delayed afterdepolarisations?

A

Excessive calcium results in oscillatory release of calcium from sarcoplasmic reticulum and a transient inward current that occurs in phase 4

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23
Q

When are delayed afterdepolarisations most likely to occur?

A

When the heart rate is fast

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24
Q

What can delayed afteredepolarisations be triggered by?

A

Drugs that increase the calcium influx or release of calcium from the sarcoplasmic reticulum (e.g. digoxin)

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25
Q

Defects in impulse conduction causing arrhythmias

A

Re-entry, conduction block (through AV node)

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26
Q

What do re-entry arrhythmias involve?

A

A self sustaining electrical circuit that stimulates an area of the myocardium repeatedly/rapidly

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27
Q

What does the re-entrant circuit require?

A

Unidirectional block and slowed retrograde conduction velocity

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28
Q

What does unidirectional block involve?

A

Anterograde conduction is prohibited and retrograde conduction is allowed (action potential goes back through in the ‘wrong’ direction in the damaged cells)

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29
Q

First degree conduction block:

  • What happens in this?
  • What will be seen on an ECG?
A
  • The tissue conducts all impulses but more slowly than usual
  • Long PR interval seen on ECG (>0.2s)
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30
Q

2 types of second degree conduction block

A

Mobitz type I, Mobitz type II

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31
Q

Describe mobitz type I conduction block

A

The PR interval gradually increases from cycle to cycle until AV node fails and a ventricular beat is missed

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32
Q

Describe mobitz type II conduction block

A

The PR interval is constant but every nth ventricular depolarisation is missing

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33
Q

Describe complete conduction block (aka third degree conduction block)

A

Atria and ventricles beat independently governed by their own pacemakers. Ventricular pacemaker is now the Purkinje fibres – fire relatively slowly and unreliably – manifest as bradycardia and low cardiac output

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34
Q

Example of accessory tract pathway

A

Bundle of Kent

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35
Q

What is an accessory tract pathway?

A

An electrical pathway in parallel to the AV node

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36
Q

Describe speed of impulse in Bundle of Kent vs AV node

A

Impulse through Bundle of Kent is conducted more quickly than the AV node

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37
Q

What happens in the ventricles with an accessory pathway

A

Ventricles receive impulses from both the normal and accessory pathways – can set up the condition for a re-entrant loop predisposing to tachyarrhythmias

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38
Q

What do anti-arrhythmic drugs generally do?

A

Inhibit specific ion channels with the intention of suppressing abnormal electrical activity

39
Q

Vaughn Williams classification of anti-arrhythmic drugs:

  • Ia - target and example
  • Ib - target and example
  • Ic - target and example
  • II - target and example
  • III - target and example
  • IV - target and example
A
  • Ia = Voltage-activated Na+ channel, e.g. Disopyramide
  • Ib = Voltage-activated Na+ channel, e.g. Lignocaine
  • Ic = Voltage-activated Na+ channel, e.g. Flecainide
  • II = beta-adrenoceptor (antagonist), e.g. Metroprolol
  • III = Voltage-activated K+ channels, e.g. Amiodarone
  • IV = Voltage-activated Ca2+ channels, e.g. Verapamil
40
Q

Action of class Ia anti-arrhythmic drugs

A

Associate with and dissociate from Na+ channels at a moderate rate. Slow rate of rise of AP and prolong refractory period

41
Q

Action of class Ib anti-arrhthymic drugs

A

Associate with and dissociate from Na+ channels at a rapid rate. Prevent premature beats

42
Q

Action of class Ic anti-arrhythmic drugs

A

Associate with and dissociate from Na+ channels at a slow rate. Depress conduction

43
Q

Action of class II anti-arrhythmic drugs

A

Decrease rate of depolarization in SA and AV nodes

44
Q

Action of class III anti-arrhythmic drugs

A

Prolong AP duration increasing refractory period

45
Q

Action of class IV anti-arrhythmic drugs

A

Slow conduction in SA and AV nodes. Decrease force of cardiac contraction

46
Q

When do class I anti-arrhythmic drugs dissociate from the sodium channel?

A

In the resting rate

47
Q

Which anti-arrhythmic drugs would you use to treat arrhythmias in the atria?

A

Classes IC, III

48
Q

Which anti-arrhythmic drugs would you use to treat arrhythmias in the ventricles

A

Classes IA, IB, II

49
Q

Which anti-arrhythmic drugs would you use to treat arrhythmias in the AV node

A

Adenosine, digoxin, classes II, IV

50
Q

Which anti-arrhythmic drugs would you use to treat arrhythmias in the atria and ventricles as well as AV accessory tract pathways

A

Amiodarone, sotalol, classes IA, IC

51
Q

What does adenosine do?

A

Activates A1-adenosine receptors coupled to Gi/o

52
Q

What does digoxin do?

A

Stimulates vagal activity

53
Q

What does verapamil do?

A

Blocks L-type voltage-activated calcium channels

54
Q

Supraventricular tachycardia types

A

Atrial fibrillation, atrial flutter, ectopic atrial tachycardia

55
Q

Ventricular arrhythmia types

A

Ventricular ectopics, ventricular tachycardia, ventricular fibrillation, asystole

56
Q

Clinical causes of arrythmias

A

Abnormal anatomy, autonomic nervous system, metabolic, inflammatory, drugs, genetic

57
Q

Causes of tachycardic arrhythmias

A

Hyperthermia, hypoxia, hypercapnia, cardiac dilation, hypokalaemia

58
Q

Causes of bradycardic arrhythmias

A

Hypothermia, hypokalaemia

59
Q

Symptoms of arrhythmia

A

Palpitations, SOB, dizziness, loss of consciousness, faintness, sudden cardiac death, angina, heart failure

60
Q

Investigations for arrhythmia and their effects

A

ECG, CXR, echocardiogram, stress ECG, 24 hour ECG, event recorder, electrophysiological study

61
Q

What do sinus arrhythmias involve?

A

Variations in heart rate, due to reflex changes in vagal tone during the respiratory cycle. Part of ECG is slow and part of the ECG shows faster. This is commonly seen in younger people/younger adults

62
Q

Sinus bradycardia:

  • What is it?
  • Causes
  • Treatment
A
  • Sinus rhythm with heart rate <60bpm
  • Causes can be physiological i.e. athletes, drugs can cause it and it can be caused by ischaemia
  • Treatment is atropine or pacing if haemodynamic compromise.
63
Q

Sinus tachycardia:

  • What is it?
  • Causes
  • Treatment
A
  • Sinus rhythm with heart rate >100bpm
  • Physiological (anxiety, fear, hypotension, anaemia), can also be caused by drugs
  • Treatment is to treat underlying cause and beta-blockers
64
Q

Atrial ectopic beats:

- Treatment

A

No treatment if asymptomatic, beta-blockers may help, avoid stimulants (caffeine, cigarettes)

65
Q

Regular supraventricular tachycardia:

  • What may it be due to?
  • Acute management
  • Chronic management
A
  • Due to AV nodal re-entrant tachycardia, AV reciprocating tachycardia, ectopic atrial tachycardia
  • Acute - Valsava manœuvre, carotid massage, IV adenosine or IV verapamil
  • Chronic - avoid stimulants, radiofrequency ablation, beta blockers, anti-arrhythmic drugs
66
Q

In which patients is radiofrequency ablation first line?

A

Young, symptomatic patients

67
Q

Radiofrequency catheter ablation

A

Selective cautery of cardiac of cardiac tissue to prevent tachycardia, targeting either an automatic focus or part of a re-entry circuit

68
Q

Radiofrequency catheter ablation procedure

A
  • ECG catheters placed in heart via femoral veins
  • Intra-cardiac ECG recorded during sinus rhythm, tachycardia and during pacing manoeuvres to find the location and mechanism of the tachycardia
  • Catheter placed over focus/pathway and tip heated to 55-65C
  • Cease antiarrhythmic drugs 3-5 days beforehand
69
Q

Causes of heart block

A

Ageing process, acute MI, myocarditis, infiltrative disease, drugs, calcific aortic valve disease, port-aorta valve surgery, genetics

70
Q

Drugs that can cause heart block

A

Beta-blockers, calcium channel blockers

71
Q

Which types of heart block indicate pacemaker requirement?

A

Mobitz type II and complete heart block

72
Q

Types of pacemakers

A

Single chamber (only paces right atria or right ventricle), dual chamber (paces both RA and RV)

73
Q

Ventricular ectopics:

  • Causes
  • Treatment
A
  • Structural causes (LVH, myocarditis, heart failure), metabolic causes (ischaemic heart disease, electrolytes)
  • Treatment is beta blockers or ablation of focus
74
Q

Ventricular tachycardia causes

A

Most patients will have significant heart disease (CAD, previous MI), other causes include cardiomyopathy, inherited/familial arrhythmia syndromes

75
Q

ECG characteristics that help define VTs

A
  • QRS complexes are wide and distorted
  • T waves are large with deflections opposite QRS complexes
  • Ventricular rhythm is usually regular
  • P waves are not usually visible
  • PR interval not measurable
76
Q

Monomorphic VT vs polymorphic VT

A

Monomorphic VT = QRS complex same all the time

Polymorphic VT = QRS complex changes all the time

77
Q

Ventricular fibrillation

A

Chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump

78
Q

Treatment for ventricular fibrillation

A

Defibrillation, CPR

79
Q

Acute treatment for ventricular tachycardia

A

Direct current cardioversion if unstable, pharmacologic cardioversion with anti-arrhythmic drugs if stable, correct triggers

80
Q

Long term treatment for ventricular tachycardia

A

Correct ischaemia if possible, optimise CHF therapies, implantable cardioverter defibrillators if life threatening, VT catheter ablation

81
Q

What is the most common arrhythmia?

A

Atrial fibrillation

82
Q

Forms of atrial fibrillation?

A

Paroxysmal, persistent, permanent

83
Q

Paroxysmal atrial fibrillation

A

Paroxysmal and lasting <48 hours, often recurrent

84
Q

Persistent atrial fibrillation

A

Episode lasting >48 hours which can still be cardioverted to sinus rhythm, however unlikely to spontaneously revert to normal sinus rhythm

85
Q

Permanent atrial fibrillation

A

Inability of pharmacologic or non-pharmacologic methods to restore to normal sinus rhythm

86
Q

Associated diseases/causes of atrial fibrillation

A

Hypertension, congestive heart failure, sick sinus syndrome, coronary heart disease, obesity, thyroid disease, familial, cardiac valve disease, alcohol abuse, congenital heart disease, cardiac surgery, COPD, pneumonia, septicaemia, pericarditis, tumours, vagal cause – high endurance athletes

87
Q

Symptoms of atrial fibrillation

A

Palpitations, Pre-syncope, Syncope, Chest pain, Dyspnoea, Sweatiness, Fatigue

88
Q

ECG changes in atrial fibrillation:

  • Atrial rate
  • Rhythm
  • Recognition
A
  • > 300bpm
  • Irregularly irregular
  • Absence of P waves and presence of ‘f’ waves
89
Q

Rate control in the treatment of AF

A

Digoxin, beta blockers, verapamil, diltiazem

90
Q

Rhythm control in the treatment of AF:

  • Restoration of normal sinus rhythm
  • Maintenance of normal sinus rhythm
A

Restoration - pharmacologic cardioversion - anti-arrhythmic drugs, direct current cardioverson
Maintenance - anti-arrhythmic drugs, catheter ablation surgery

91
Q

Indications for anticoagulation in AF

A

Thyrotoxicosis, hypertrophic cardiomyopathy, valvular AF (warfarin only), non-valvular AF with 2 or more risk factors (age >75, hypertension, heart failure, previous stroke, diabetes, CAD

92
Q

Atrial flutter:

  • What is it?
  • What is it sustained by?
  • How long does it last?
  • What may it result in?
A
  • Rapid and regular form of atrial tachycardia, which is usually paroxysmal
  • Sustained by a macro-re-entrant circuit confined to the rate atrium
  • Episodes last seconds to years
  • Can result in thrombo-embolism
93
Q

Treatment for atrial flutter

A

Radiofrequency ablation, pharmacologic therapy, cardioversion, warfarin for prevention of thromboembolism

Medicine Cardiovascular (24 decks)

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